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The Effect of Mebudipine on Cardiac Function and Activity of the Myocardial Nitric Oxide System in Ischaemia-Reperfusion Injury in Rats Publisher Pubmed



Ghyasi R1 ; Mohammadi M2 ; Badalzadeh R2, 3 ; Rashidi B4 ; Sepehri G1
Authors
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Authors Affiliations
  1. 1. Physiology and Neuroscience Research Centre, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran
  2. 2. Department of Physiology, Drug Applied Research Centre, Tabriz University of Medical Sciences, Iran
  3. 3. Young Researchers Club of Tabriz, Islamic Azad University, Tabriz, Iran
  4. 4. Department of Anatomy, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Cardiovascular Journal of Africa Published:2011


Abstract

Objectives: Previous studies have suggested that failure of the synthesis of nitric oxide is involved in the pathophysiology of myocardial ischaemia-reperfusion injury. In this study, we investigated the effect of mebudipine, a new dihydropyridine calcium channel blocker, on cardiac function and activity of the myocardial nitric oxide system in ischaemia-reperfusion injury in isolated rat hearts. Methods: Forty male Wistar rats (250-300 g) were divided into four groups (n = 10): sham, control, vehicle and drug groups. The animals were anesthetised with sodium pentobarbital (6 mg/kg intraperitoneal). The hearts were quickly removed, mounted on a Longendorff apparatus and perfused with Krebs-Henseleit solution under constant pressure at 37° C. After 20 min stabilisation period, the ischaemic groups received 30 min global ischaemia and 120 min reperfusion. For the drug and vehicle groups, before ischaemia the hearts were perfused with mebudipine (10-3 μM) or ethanol-enriched solution (0.01%) for 25 min, respectively. Myocardial function, and creatine kinase, lactate dehydogenase and total nitric oxide metabolite (nitrite and nitrate) levels were analysed. Results: Cardiac functions had recovered significantly in the mebudipine group (p 〈 0.01). Furthermore, mebudipine remarkably reduced the levels of lactate dehydogenase and creatine kinase in the coronary effluent and increased myocardial nitric oxide metabolite levels compared with the control group. Conclusion: Our results indicate that mebudipine reduced the intensity of myocardial ischaemia-reperfusion injury, and that activation of the myocardial nitric oxide system played an important role in this regard.
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